Evidence map›Paper›PMID 17296927›Full record

ArticleThe Journal of general physiology2007

Corelease and differential exit via the fusion pore of GABA, serotonin, and ATP from LDCV in rat pancreatic beta cells.

Matthias Braun, Anna Wendt, Jovita Karanauskaite, Juris Galvanovskis, Anne Clark, Patrick E MacDonald, Patrik Rorsman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
7.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

51 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Metabolic and Molecular Amplification of Insulin Secretion.Advances in anatomy, embryology, and cell biology · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. The role of GABA in islet function.Frontiers in endocrinology · 2022
    Review
  9. Review
  10. Article
  11. Purinergic signaling in diabetes and metabolism.Biochemical pharmacology · 2021
    Review
  12. Review
  13. Article
  14. Regulating quantal size of neurotransmitter release through a GPCR voltage sensor.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  15. Ion Channels of the Islets in Type 2 Diabetes.Journal of molecular biology · 2020
    Review
  16. Purinergic signaling in hepatic disease.Purinergic signalling · 2019
    Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Matthias BraunOxford Center for Diabetes, Endocrinology, and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, UK. matthias.braun@drl.ox.ac.uk
Anna Wendt
Jovita Karanauskaite
Juris Galvanovskis
Anne Clark
Patrick E MacDonald
Patrik Rorsman
Churchill Hospital · GBLund University · SE

Funding

Wellcome TrustWellcome Trust WT072289
6 · The paper itself

Abstract

The release of gamma-aminobutyric acid (GABA) and ATP from rat beta cells was monitored using an electrophysiological assay based on overexpression GABA(A) or P2X2 receptor ion channels. Exocytosis of LDCVs, detected by carbon fiber amperometry of serotonin, correlated strongly (approximately 80%) with ATP release. The increase in membrane capacitance per ATP release event was 3.4 fF, close to the expected capacitance of an individual LDCV with a diameter of 0.3 microm. ATP and GABA were coreleased with serotonin with the same probability. Immunogold electron microscopy revealed that approximately 15% of the LDCVs contain GABA. Prespike "pedestals," reflecting exit of granule constituents via the fusion pore, were less frequently observed for ATP than for serotonin or GABA and the relative amplitude (amplitude of foot compared to spike) was smaller: in some cases the ATP-dependent pedestal was missing entirely. An inward tonic current, not dependent on glucose and inhibited by the GABA(A) receptor antagonist SR95531, was observed in beta cells in clusters of islet cells. Noise analysis indicated that it was due to the activity of individual channels with a conductance of 30 pS, the same as expected for individual GABA(A) Cl- channels with the ionic gradients used. We conclude that (a) LDCVs accumulate ATP and serotonin; (b) regulated release of GABA can be accounted for by exocytosis of a subset of insulin-containing LDCVs; (c) the fusion pore of LDCVs exhibits selectivity and compounds are differentially released depending on their chemical properties (including size); and (d) a glucose-independent nonvesicular form of GABA release exists in beta cells.

Indexed as

Adenosine TriphosphateAnimalsExocytosisGABA-A Receptor Antagonistsgamma-Aminobutyric AcidInsulin-Secreting CellsKineticsMembrane FusionMicroscopy, ImmunoelectronModels, BiologicalMolecular WeightPurinergic P2 Receptor AntagonistsPyridazinesRatsReceptors, Purinergic P2X2Secretory VesiclesAdenosine TriphosphateGABA-A Receptor Antagonistsgabazinegamma-Aminobutyric AcidP2rx2 protein, ratPurinergic P2 Receptor AntagonistsPyridazinesReceptors, Purinergic P2X2Serotonin

Identifiers

PMID17296927
PMCPMC2151613
OpenAlexW2103829969

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.